The influence of blood flow changes in secretion in the stomach has not been defined. The chemical mediator of vasodilation in the gastric circulation is unknown. We propose to investigate these physiological questions. Our operating hypotheses will be: 1) increasing blood flow alone in the secreting stomach will increase secretion by delivering more secretagogue per unit time, whereas increasing blood flow per se will not initiate secretion in the resting stomach; and 2) cyclic AMP is the intracellular chemical mediator of vasodilation in the gastric artterial wall; accumulation of this nucleotide by vasodilators occurs by two mechanisms, namely inhibition of the cycle AMP degrading enzyme, phosphodiesterase, or by activation of the biosynthetic enzyme, adenylate cyclase. We will test the first hypothesis by measuring mucosal clearance of aminopyrine, gastroepiploic artery blood flow and gastric secretion in an anesthetized dog preparation in response to intraarterial infusion of vasoactive drugs which do not, of themselves, stimulate or inhibit gastric secretion. We will test the second hypothesis by measuring gastric arterial wall cyclic AMP content, phosphodiesterase and adenylate cyclase activity, ATP content and blood flow in response to vasodilator drugs.